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BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex [ATAC-seq]

ABSTRACT: BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex [ATAC-seq]

PROVIDER: PRJNA692734 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13450600.fastq.gz	Fastqsanger.gz
	SRR13450600_1.fastq.gz	Fastqsanger.gz
	SRR13450600_2.fastq.gz	Fastqsanger.gz
	SRR13450601.fastq.gz	Fastqsanger.gz
	SRR13450601_1.fastq.gz	Fastqsanger.gz

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BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex [RNA-seq]

Project description:mSWI/SNF or BAF chromatin regulatory complexes are dosage-sensitive regulators of human neural development frequently mutated in autism and intellectual disability. Cell cycle exit and differentiation of neural stem/progenitor cells is accompanied by BAF subunit switching to generate neuron-specific nBAF complexes. We manipulated the timing of BAF subunit exchange in vivo and found that early loss of the npBAF subunit BAF53a stalls cell cycle exit to disrupt neurogenesis. Loss of BAF53a results in decreased chromatin accessibility at specific neural transcription factor binding sites, including the pioneer factors Sox2 and Ascl1, due to Polycomb accumulation. This results in repression of cell cycle genes, thereby blocking cell cycle progression and differentiation. Cell cycle block upon Baf53a deletion could be rescued by premature expression of the nBAF subunit BAF53b but not by other major drivers of proliferation or differentiation. Wnt, EGF, FGF, Sox2, myc or Pax6 all fail to maintain proliferation in the absence of BAF53a, highlighting a novel mechanism underlying neural progenitor cell cycle exit in the continued presence of extrinsic proliferative cues.

2021-01-18 | GSE164990 | GEO

BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex [ATAC-seq]

2021-01-18 | GSE164989 | GEO

BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex

Project description:BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex

| PRJNA692733 | ENA

BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex [RNA-seq]

Project description:BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex [RNA-seq]

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BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex.

Project description:mSWI/SNF or BAF chromatin regulatory complexes are dosage-sensitive regulators of human neural development frequently mutated in autism spectrum disorders and intellectual disability. Cell cycle exit and differentiation of neural stem/progenitor cells is accompanied by BAF subunit switching to generate neuron-specific nBAF complexes. We manipulated the timing of BAF subunit exchange in vivo and found that early loss of the npBAF subunit BAF53a stalls the cell cycle to disrupt neurogenesis. Loss of BAF53a results in decreased chromatin accessibility at specific neural transcription factor binding sites, including the pioneer factors SOX2 and ASCL1, due to Polycomb accumulation. This results in repression of cell cycle genes, thereby blocking cell cycle progression and differentiation. Cell cycle block upon Baf53a deletion could be rescued by premature expression of the nBAF subunit BAF53b but not by other major drivers of proliferation or differentiation. WNT, EGF, bFGF, SOX2, c-MYC, or PAX6 all fail to maintain proliferation in the absence of BAF53a, highlighting a novel mechanism underlying neural progenitor cell cycle exit in the continued presence of extrinsic proliferative cues.

| S-EPMC7919417 | biostudies-literature

BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-18 | GSE164991 | GEO

Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders

Project description:The BAF complex modulates chromatin accessibility. Specific BAF configurations have functional consequences, and subunit switches are essential for cell differentiation. ARID1B and its paralog ARID1A encode for mutually exclusive BAF subunits. De novo ARID1B haploinsufficient mutations cause a neurodevelopmental disorder spectrum, including Coffin-Siris syndrome, which is characterized by neurological and craniofacial features. Here, we reprogrammed ARID1B+/- Coffin-Siris patient-derived skin fibroblasts into iPSCs, and modeled cranial neural crest cell (CNCC) formation. We discovered that ARID1B is active only during the first stage of this process, coinciding with neuroectoderm specification, where it is part of a lineage-specific BAF configuration (ARID1B-BAF), including SMARCA4, and nine additional subunits. ARID1B-BAF acts as a gate-keeper, ensuring exit from pluripotency and lineage commitment, by attenuating NANOG, SOX2 and the thousands of enhancers directly regulated by these two pluripotency factors at the iPSC stage. In iPSCs, these enhancers are maintained active by an ARID1A-containing BAF. At the onset of differentiation, cells transition from ARID1A-BAF to ARID1B-BAF, eliciting attenuation of the NANOG/SOX2 networks, and triggering pluripotency exit. Coffin-Siris patient cells fail to perform the ARID1A/ARID1B switch, and maintain ARID1A-BAF at pluripotency enhancers throughout all stages of CNCC formation. This leads to a persistent and aberrant SOX2 and NANOG activity, which impairs CNCC formation. In fact, despite showing the typical neural crest signature (TFAP2A+, SOX9+), the ARID1B-haploinsufficient CNCCs are also NANOG-positive, in stark contrast with the ARID1B-wt CNCCs, which are NANOG-negative. These findings suggest a connection between ARID1B mutations, neuroectoderm formation, and a pathogenic mechanism for Coffin-Siris syndrome.

2021-10-12 | PXD028557 | Pride

Ribonucleotide Reductase Subunit Switching in Hepatoblastoma Drug Response and Relapse

Project description:To investigate the effect of RNR subunit switching in relation to Drug Resistance in hepatoblastoma

2023-02-13 | GSE223839 | GEO

Dynamic BAF chromatin remodeling complex subunit inclusion promotes temporally distinct gene expression programs in cardiogenesis

Project description:Chromatin remodeling complexes instruct cellular differentiation and lineage specific transcription. The BRG1/BRM associated factor (BAF) complexes are important for several aspects of differentiation. We show that the catalytic subunit Brg1 has a specific role in cardiac precursors (CPs) to initiate cardiac gene expression programs and repress non-cardiac expression. Using immunoprecipitation immunopurification with mass spectrometry we determined the dynamic composition of BAF complexes during mammalian cardiac differentiation, identifying several cell-type specific subunits. We focused on the CP- and cardiomyocytes (CM)-enriched subunits BAF60c (SMARCD3) and BAF170 (SMARCC2). Baf60c and Baf170 co-regulate gene expression with Brg1 in CPs, and in CMs their loss results in broadly deregulated cardiac gene expression. BRG1, BAF60, and BAF170 modulate chromatin accessibility, to either promote accessibility at activated genes, while closing up chromatin at repressed genes. BAF60c and BAF170 are required for proper BAF complex composition, and BAF170 loss leads to retention of BRG1 at CP-specific enhancers. Thus, dynamic interdependent BAF complex subunit assembly modulates chromatin states and thereby participates in directing temporal gene expression programs in cardiogenesis.

2019-11-13 | PXD012721 | Pride

Ribonucleotide Reductase Subunit Switching in Hepatoblastoma Drug Response and Relapse

Project description:Ribonucleotide Reductase Subunit Switching in Hepatoblastoma Drug Response and Relapse

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